Marijuana cannabinoids slow brain degradation and aging, reverse dementia

[RainDog]

59. The article they cite comes from the foremost scientific asso. in Britain

this organization - http://rstb.royalsocietypublishing.org/

Each issue of Philosophical Transactions B is devoted to a specific area of the biological sciences, and aims to define a research frontier that is advancing rapidly, often bridging traditional disciplines. Each issue is guest edited by one or more experts in the field. All contributions are invited and the journal does not accept unsolicited stand-alone papers.

The Royal Society is the equivalent of the National Academy of Sciences in the U.S. The most prestigious scientific organization in the UK.

Here's a link to the introduction to the Society's Report on the cutting edge of endocannabinoid research:

Endocannabinoids in nervous system health and disease

http://rstb.royalsocietypublishing.org/site/2012/endocannabinoids.xhtml

The link also has a video that talks about the journal issue and the focus of research.

You can't just dismiss something because information appears in one context. You need to look at the information itself to determine whether the information is woo or is, in fact, one of the major topics/questions in scientific research.

Here's an article that discusses the issue from a peer-reviewed journal:

http://www.ncbi.nlm.nih.gov/pubmed/17140265

A molecular link between the active component of marijuana and Alzheimer's disease pathology.

Abstract
Alzheimer's disease is the leading cause of dementia among the elderly, and with the ever-increasing size of this population, cases of Alzheimer's disease are expected to triple over the next 50 years. Consequently, the development of treatments that slow or halt the disease progression have become imperative to both improve the quality of life for patients and reduce the health care costs attributable to Alzheimer's disease. Here, we demonstrate that the active component of marijuana, Delta9-tetrahydrocannabinol (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as well as prevents AChE-induced amyloid beta-peptide (Abeta) aggregation, the key pathological marker of Alzheimer's disease. Computational modeling of the THC-AChE interaction revealed that THC binds in the peripheral anionic site of AChE, the critical region involved in amyloidgenesis. Compared to currently approved drugs prescribed for the treatment of Alzheimer's disease, THC is a considerably superior inhibitor of Abeta aggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may directly impact the progression of this debilitating disease.